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Article ; Online: Bench-to-Bedside Studies of Arginine Deprivation in Cancer.

Field, George C / Pavlyk, Iuliia / Szlosarek, Peter W

2023 Volume 28, Issue 5

Abstract: Arginine is a semi-essential amino acid which becomes wholly essential in many cancers commonly due to the functional loss of Argininosuccinate Synthetase 1 (ASS1). As arginine is vital for a plethora of cellular processes, its deprivation provides a ... ...

Abstract	Arginine is a semi-essential amino acid which becomes wholly essential in many cancers commonly due to the functional loss of Argininosuccinate Synthetase 1 (ASS1). As arginine is vital for a plethora of cellular processes, its deprivation provides a rationale strategy for combatting arginine-dependent cancers. Here we have focused on pegylated arginine deiminase (ADI-PEG20, pegargiminase)-mediated arginine deprivation therapy from preclinical through to clinical investigation, from monotherapy to combinations with other anticancer therapeutics. The translation of ADI-PEG20 from the first in vitro studies to the first positive phase 3 trial of arginine depletion in cancer is highlighted. Finally, this review discusses how the identification of biomarkers that may denote enhanced sensitivity to ADI-PEG20 beyond ASS1 may be realized in future clinical practice, thus personalising arginine deprivation therapy for patients with cancer.
MeSH term(s)	Humans ; Arginine/metabolism ; Cell Line, Tumor ; Argininosuccinate Synthase/metabolism ; Hydrolases ; Polyethylene Glycols/therapeutic use ; Neoplasms/drug therapy
Chemical Substances	Arginine (94ZLA3W45F) ; Argininosuccinate Synthase (EC 6.3.4.5) ; Hydrolases (EC 3.-) ; Polyethylene Glycols (3WJQ0SDW1A)
Language	English
Publishing date	2023-02-24
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules28052150
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Article: Arginine Deprivation in SCLC: Mechanisms and Perspectives for Therapy.

Carpentier, Joséphine / Pavlyk, Iuliia / Mukherjee, Uma / Hall, Peter E / Szlosarek, Peter W

Lung Cancer (Auckland, N.Z.)

2022 Volume 13, Page(s) 53–66

Abstract: Arginine deprivation has gained increasing traction as a novel and safe antimetabolite strategy for the treatment of several hard-to-treat cancers characterised by a critical dependency on arginine. Small cell lung cancer (SCLC) displays marked arginine ... ...

Abstract	Arginine deprivation has gained increasing traction as a novel and safe antimetabolite strategy for the treatment of several hard-to-treat cancers characterised by a critical dependency on arginine. Small cell lung cancer (SCLC) displays marked arginine auxotrophy due to inactivation of the rate-limiting enzyme argininosuccinate synthetase 1 (ASS1), and as a consequence may be targeted with pegylated arginine deiminase or ADI-PEG20 (pegargiminase) and human recombinant pegylated arginases (rhArgPEG, BCT-100 and pegzilarginase). Although preclinical studies reveal that ASS1-deficient SCLC cell lines are highly sensitive to arginine-degrading enzymes, there is a clear disconnect with the clinic with minimal activity seen to date that may be due in part to patient selection. Recent studies have explored resistance mechanisms to arginine depletion focusing on tumor adaptation, such as ASS1 re-expression and autophagy, stromal cell inputs including macrophage infiltration, and tumor heterogeneity. Here, we explore how arginine deprivation may be combined strategically with novel agents to improve SCLC management by modulating resistance and increasing the efficacy of existing agents. Moreover, recent work has identified an intriguing role for targeting arginine in combination with PD-1/PD-L1 immune checkpoint inhibitors and clinical trials are in progress. Thus, future studies of arginine-depleting agents with chemoimmunotherapy, the current standard of care for SCLC, may lead to enhanced disease control and much needed improvements in long-term survival for patients.
Language	English
Publishing date	2022-09-05
Publishing country	New Zealand
Document type	Journal Article ; Review
ZDB-ID	2587467-6
ISSN	1179-2728
ISSN	1179-2728
DOI	10.2147/LCTT.S335117
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Article ; Online: Optimizing arginine deprivation for hard-to-treat cancers.

Khadeir, Ramsay / Szyszko, Teresa / Szlosarek, Peter W

Oncotarget

2017 Volume 8, Issue 57, Page(s) 96468–96469

Language	English
Publishing date	2017-11-14
Publishing country	United States
Document type	Editorial
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.22099
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Article ; Online: A role for macrophages under cytokine control in mediating resistance to ADI-PEG20 (pegargiminase) in ASS1-deficient mesothelioma.

Phillips, Melissa M / Pavlyk, Iuliia / Allen, Michael / Ghazaly, Essam / Cutts, Rosalind / Carpentier, Josephine / Berry, Joe Scott / Nattress, Callum / Feng, Shenghui / Hallden, Gunnel / Chelala, Claude / Bomalaski, John / Steele, Jeremy / Sheaff, Michael / Balkwill, Frances / Szlosarek, Peter W

Pharmacological reports : PR

2023 Volume 75, Issue 3, Page(s) 570–584

Abstract: Background: Pegylated arginine deiminase (ADI-PEG20; pegargiminase) depletes arginine and improves survival outcomes for patients with argininosuccinate synthetase 1 (ASS1)-deficient malignant pleural mesothelioma (MPM). Optimisation of ADI-PEG20-based ... ...

Abstract	Background: Pegylated arginine deiminase (ADI-PEG20; pegargiminase) depletes arginine and improves survival outcomes for patients with argininosuccinate synthetase 1 (ASS1)-deficient malignant pleural mesothelioma (MPM). Optimisation of ADI-PEG20-based therapy will require a deeper understanding of resistance mechanisms, including those mediated by the tumor microenvironment. Here, we sought to reverse translate increased tumoral macrophage infiltration in patients with ASS1-deficient MPM relapsing on pegargiminase therapy. Methods: Macrophage-MPM tumor cell line (2591, MSTO, JU77) co-cultures treated with ADI-PEG20 were analyzed by flow cytometry. Microarray experiments of gene expression profiling were performed in ADI-PEG20-treated MPM tumor cells, and macrophage-relevant genetic "hits" were validated by qPCR, ELISA, and LC/MS. Cytokine and argininosuccinate analyses were performed using plasma from pegargiminase-treated patients with MPM. Results: We identified that ASS1-expressing macrophages promoted viability of ADI-PEG20-treated ASS1-negative MPM cell lines. Microarray gene expression data revealed a dominant CXCR2-dependent chemotactic signature and co-expression of VEGF-A and IL-1α in ADI-PEG20-treated MPM cell lines. We confirmed that ASS1 in macrophages was IL-1α-inducible and that the argininosuccinate concentration doubled in the cell supernatant sufficient to restore MPM cell viability under co-culture conditions with ADI-PEG20. For further validation, we detected elevated plasma VEGF-A and CXCR2-dependent cytokines, and increased argininosuccinate in patients with MPM progressing on ADI-PEG20. Finally, liposomal clodronate depleted ADI-PEG20-driven macrophage infiltration and suppressed growth significantly in the MSTO xenograft murine model. Conclusions: Collectively, our data indicate that ADI-PEG20-inducible cytokines orchestrate argininosuccinate fuelling of ASS1-deficient mesothelioma by macrophages. This novel stromal-mediated resistance pathway may be leveraged to optimize arginine deprivation therapy for mesothelioma and related arginine-dependent cancers.
MeSH term(s)	Animals ; Humans ; Mice ; Arginine/metabolism ; Argininosuccinate Synthase/genetics ; Argininosuccinate Synthase/metabolism ; Cell Line, Tumor ; Mesothelioma/drug therapy ; Mesothelioma/genetics ; Mesothelioma, Malignant ; Neoplasm Recurrence, Local ; Polyethylene Glycols/pharmacology ; Tumor Microenvironment ; Vascular Endothelial Growth Factor A ; Macrophages ; Drug Resistance, Neoplasm
Chemical Substances	ADI PEG20 (EC 3.5.3.6) ; Arginine (94ZLA3W45F) ; Argininosuccinate Synthase (EC 6.3.4.5) ; Polyethylene Glycols (3WJQ0SDW1A) ; Vascular Endothelial Growth Factor A
Language	English
Publishing date	2023-04-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2186248-5
ISSN	2299-5684 ; 1734-1140
ISSN (online)	2299-5684
ISSN	1734-1140
DOI	10.1007/s43440-023-00480-6
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Article ; Online: Correction: A role for macrophages under cytokine control in mediating resistance to ADI-PEG20 (pegargiminase) in ASS1-deficient mesothelioma.

Pharmacological reports : PR

2023 Volume 75, Issue 3, Page(s) 753

Language	English
Publishing date	2023-05-17
Publishing country	Switzerland
Document type	Published Erratum
ZDB-ID	2186248-5
ISSN	2299-5684 ; 1734-1140
ISSN (online)	2299-5684
ISSN	1734-1140
DOI	10.1007/s43440-023-00487-z
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Article ; Online: BAP1 Loss Is Associated with Higher ASS1 Expression in Epithelioid Mesothelioma: Implications for Therapeutic Stratification.

Barnett, Sarah E / Kenyani, Jenna / Tripari, Martina / Butt, Zohra / Grosman, Rudi / Querques, Francesca / Shaw, Liam / Silva, Luisa C / Goate, Zoe / Marciniak, Stefan J / Rassl, Doris M / Jackson, Richard / Lian, Lu-Yun / Szlosarek, Peter W / Sacco, Joseph J / Coulson, Judy M

Molecular cancer research : MCR

2023 Volume 21, Issue 5, Page(s) 411–427

Abstract: The nuclear deubiquitylase BRCA1-associated protein 1 (BAP1) is frequently inactivated in malignant pleural mesothelioma (MPM) and germline BAP1 mutation predisposes to cancers including MPM. To explore the influence on cell physiology and drug ... ...

Abstract	The nuclear deubiquitylase BRCA1-associated protein 1 (BAP1) is frequently inactivated in malignant pleural mesothelioma (MPM) and germline BAP1 mutation predisposes to cancers including MPM. To explore the influence on cell physiology and drug sensitivity, we sequentially edited a predisposition mutation (w-) and a promoter trap (KO) into human mesothelial cells. BAP1w-/KO MeT5A cells express less BAP1 protein and phenocopy key aspects of BAP1 loss in MPM. Stable isotope labeling with amino acids in cell culture-mass spectrometry revealed evidence of metabolic adaptation, with concomitant alteration of cellular metabolites. In MeT5A, BAP1 deficiency reduces glycolytic enzyme levels but increases enzymes involved in the tricarboxylic acid cycle and anaplerotic pathways. Notably both argininosuccinate synthase 1 (ASS1), essential for cellular synthesis of arginine, and its substrate aspartate, are elevated in BAP1w-/KO MeT5A cells. Likewise, ASS1 expression is higher in BAP1-altered MPM cell lines, and inversely correlates with BAP1 in The Cancer Genome Atlas MESO dataset. Elevated ASS1 is also evident by IHC staining in epithelioid MPM lacking nuclear BAP1 expression, with improved survival among patients with BAP1-negative/ASS1-expressing tumors. Alterations in arginine metabolism may sensitize cells to metabolic drugs and we find that BAP1-negative/ASS1-expressing MPM cell lines are more sensitive to ASS1 inhibition, although not to inhibition of purine synthesis by mizoribine. Importantly, BAP1w-/KO MeT5A become desensitized to arginine deprivation by pegylated arginine deiminase (ADI-PEG20), phenocopying BAP1-negative/ASS1-expressing MPM cell lines. Implications: Our data reveal an interrelationship between BAP1 and arginine metabolism, providing a potential means of identifying patients with epithelioid MPM likely to benefit from ADI-PEG20.
MeSH term(s)	Humans ; Mesothelioma, Malignant ; Argininosuccinate Synthase/genetics ; Argininosuccinate Synthase/metabolism ; Ubiquitin Thiolesterase/genetics ; Amino Acids ; Arginine/metabolism ; Mesothelioma/drug therapy ; Mesothelioma/genetics ; Cell Line, Tumor ; Tumor Suppressor Proteins/genetics
Chemical Substances	Argininosuccinate Synthase (EC 6.3.4.5) ; Ubiquitin Thiolesterase (EC 3.4.19.12) ; Amino Acids ; Arginine (94ZLA3W45F) ; BAP1 protein, human ; Tumor Suppressor Proteins
Language	English
Publishing date	2023-01-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-22-0635
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Article ; Online: Role of 3'-Deoxy-3'-[

Szyszko, Teresa A / Dunn, Joel T / Phillips, Melissa M / Bomalaski, John / Sheaff, Michael T / Ellis, Steve / Pike, Lucy / Goh, Vicky / Cook, Gary J R / Szlosarek, Peter W

JTO clinical and research reports

2022 Volume 3, Issue 9, Page(s) 100382

Abstract: Introduction: Pegargiminase (ADI-PEG 20I) degrades arginine in patients with argininosuccinate synthetase 1-deficient malignant pleural mesothelioma (MPM) and NSCLC. Imaging with proliferation biomarker 3'-deoxy-3'-[: Methods: A total of 18 patients ... ...

Abstract	Introduction: Pegargiminase (ADI-PEG 20I) degrades arginine in patients with argininosuccinate synthetase 1-deficient malignant pleural mesothelioma (MPM) and NSCLC. Imaging with proliferation biomarker 3'-deoxy-3'-[ Methods: A total of 18 patients with thoracic malignancies (10 MPM; eight NSCLC) underwent imaging. FLT PET-CT was performed at baseline (PET1), 24 hours post-pegargiminase monotherapy (PET2), post one cycle of ADIPemCis (PET3), and at end of treatment (EOT, PET4). CT was performed at baseline (CT1) and EOT (CT4). CT4 (modified) Response Evaluation Criteria in Solid Tumors (RECIST) response was compared with treatment response on PET (changes in maximum standardized uptake value [SUVmax] on European Organisation for Research and Treatment of Cancer-based criteria). Categorical responses (progression, partial response, and stable disease) for PET2, PET3, and PET4 were compared against CT using Cohen's kappa. Results: ADIPemCis treatment response resulted in 22% mean decrease in size between CT1 and CT4 and 37% mean decrease in SUVmax between PET1 and PET4. PET2 agreed with CT4 response in 62% (8 of 13) of patients ( Conclusions: Early FLT imaging (PET2) agrees with EOT CT results in nearly two-thirds of patients. Both early and late FLT PET-CT provide evidence of response to ADIPemCis therapy in MPM and NSCLC. We provide first-in-human FLT PET-CT data in MPM, indicating it is comparable with modified RECIST.
Language	English
Publishing date	2022-07-20
Publishing country	United States
Document type	Journal Article
ISSN	2666-3643
ISSN (online)	2666-3643
DOI	10.1016/j.jtocrr.2022.100382
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Article ; Online: A Phase 1 study of ADI-PEG20 (pegargiminase) combined with cisplatin and pemetrexed in ASS1-negative metastatic uveal melanoma.

Chan, Pui Ying / Phillips, Melissa M / Ellis, Stephen / Johnston, Amanda / Feng, Xiaoxing / Arora, Amit / Hay, Gordon / Cohen, Victoria M L / Sagoo, Mandeep S / Bomalaski, John S / Sheaff, Michael T / Szlosarek, Peter W

Pigment cell & melanoma research

2022 Volume 35, Issue 4, Page(s) 461–470

Abstract: Metastatic uveal melanoma (UM) is a devastating disease with few treatment options. We evaluated the safety, tolerability and preliminary activity of arginine depletion using pegylated arginine deiminase (ADI-PEG20; pegargiminase) combined with ... ...

Abstract	Metastatic uveal melanoma (UM) is a devastating disease with few treatment options. We evaluated the safety, tolerability and preliminary activity of arginine depletion using pegylated arginine deiminase (ADI-PEG20; pegargiminase) combined with pemetrexed (Pem) and cisplatin (Cis) chemotherapy in a phase 1 dose-expansion study of patients with argininosuccinate synthetase (ASS1)-deficient metastatic UM. Eligible patients received up to six cycles of Pem (500 mg/m
MeSH term(s)	Arginine ; Argininosuccinate Synthase ; Cisplatin/therapeutic use ; Humans ; Hydrolases ; Melanoma/drug therapy ; Neoplasms, Second Primary ; Pemetrexed/therapeutic use ; Polyethylene Glycols ; Uveal Neoplasms
Chemical Substances	Pemetrexed (04Q9AIZ7NO) ; Polyethylene Glycols (3WJQ0SDW1A) ; Arginine (94ZLA3W45F) ; Hydrolases (EC 3.-) ; ADI PEG20 (EC 3.5.3.6) ; Argininosuccinate Synthase (EC 6.3.4.5) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2022-05-16
Publishing country	England
Document type	Clinical Trial, Phase I ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2409570-9
ISSN	1755-148X ; 1600-0749 ; 0893-5785 ; 1755-1471
ISSN (online)	1755-148X ; 1600-0749
ISSN	0893-5785 ; 1755-1471
DOI	10.1111/pcmr.13042
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Zs.A 2444: Show issues

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Article ; Online: Phase II Study of Arginine Deprivation Therapy With Pegargiminase in Patients With Relapsed Sensitive or Refractory Small-cell Lung Cancer.

Hall, Peter E / Ready, Neal / Johnston, Amanda / Bomalaski, John S / Venhaus, Ralph R / Sheaff, Michael / Krug, Lee / Szlosarek, Peter W

Clinical lung cancer

2020 Volume 21, Issue 6, Page(s) 527–533

Abstract: Background: Pre-clinical studies indicated that arginine-deprivation therapy using pegylated arginine deiminase (pegargiminase, ADI-PEG 20) may be effective in patients with argininosuccinate synthetase 1 (ASS1)-deficient small-cell lung cancer (SCLC).!# ...

Abstract	Background: Pre-clinical studies indicated that arginine-deprivation therapy using pegylated arginine deiminase (pegargiminase, ADI-PEG 20) may be effective in patients with argininosuccinate synthetase 1 (ASS1)-deficient small-cell lung cancer (SCLC). Patients and methods: Patients were enrolled into either a 'sensitive' disease cohort (≥ 90 days response to first-line chemotherapy) or a 'refractory' disease cohort (progression while on chemotherapy or < 90 days afterwards or ≥ third-line treatment). Patients received weekly intramuscular pegargiminase, 320 IU/m Results: Between January 2011 and January 2014, 22 patients were enrolled: 9 in the sensitive disease cohort and 13 in the refractory disease cohort. At a pre-planned interim analysis, the best overall response observed was stable disease in 2 patients in each cohort (18.2%). Owing to the lack of response and slow accrual in the sensitive disease cohort, the study was terminated early. Pegargiminase treatment was well-tolerated with no unexpected adverse events or discontinuations. Conclusion: Although pegargiminase monotherapy in SCLC failed to meet its primary endpoint of RECIST-confirmed responses, more recent molecular stratification, including MYC status, may provide new opportunities moving forward.
MeSH term(s)	Aged ; Aged, 80 and over ; Arginine/deficiency ; Case-Control Studies ; Drug Resistance, Neoplasm ; Female ; Follow-Up Studies ; Humans ; Hydrolases/therapeutic use ; Lung Neoplasms/drug therapy ; Lung Neoplasms/pathology ; Male ; Middle Aged ; Neoplasm Recurrence, Local/drug therapy ; Neoplasm Recurrence, Local/pathology ; Non-Randomized Controlled Trials as Topic ; Polyethylene Glycols/therapeutic use ; Prognosis ; Retrospective Studies ; Salvage Therapy ; Small Cell Lung Carcinoma/drug therapy ; Small Cell Lung Carcinoma/pathology
Chemical Substances	Polyethylene Glycols (3WJQ0SDW1A) ; Arginine (94ZLA3W45F) ; Hydrolases (EC 3.-) ; ADI PEG20 (EC 3.5.3.6)
Language	English
Publishing date	2020-07-30
Publishing country	United States
Document type	Clinical Trial, Phase II ; Journal Article ; Multicenter Study ; Research Support, Non-U.S. Gov't
ZDB-ID	2145146-1
ISSN	1938-0690 ; 1525-7304
ISSN (online)	1938-0690
ISSN	1525-7304
DOI	10.1016/j.cllc.2020.07.012
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Zs.MO 440: Show issues

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Article ; Online: Rewiring mitochondrial pyruvate metabolism: switching off the light in cancer cells?

Szlosarek, Peter W / Lee, SukJun / Pollard, Patrick J

Molecular cell

2014 Volume 56, Issue 3, Page(s) 343–344

Abstract: Metabolic reprogramming is a characteristic of cancer cells. Three studies published in this month's Molecular Cell provide novel insights into the role of mitochondrial pyruvate in tumor metabolism and describe how targeting pyruvate transport and ... ...

Abstract	Metabolic reprogramming is a characteristic of cancer cells. Three studies published in this month's Molecular Cell provide novel insights into the role of mitochondrial pyruvate in tumor metabolism and describe how targeting pyruvate transport and metabolism may afford therapeutic benefit.
MeSH term(s)	Biological Transport ; Glycolysis ; Humans ; Mitochondria/metabolism ; Molecular Targeted Therapy ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Neoplasms/pathology ; Pyruvic Acid/metabolism
Chemical Substances	Pyruvic Acid (8558G7RUTR)
Language	English
Publishing date	2014-11-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2014.10.018
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